Exposure to a hot environment can activate rostral ventrolateral medulla‐projecting neurones in the hypothalamic paraventricular nucleus in conscious rats

Cham, Joo Lee; Badoer, Emilio

doi:10.1113/expphysiol.2007.039560

Cited by 18 publications

(18 citation statements)

References 52 publications

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“…Recently, we have found that neurons in the PVN that project to the spinal cord or to the RVLM are among the populations of neurons that are activated when body temperature is increased (9,11). Indeed, the proportion of spinal projecting neurons in the PVN that were activated by hyperthermia was Ͼ 20% and is higher than many stimuli examined to date.…”

Section: Discussionmentioning

confidence: 99%

“…This indicates that sympathetic nerves innervating those tissues are connected polysynaptically to the PVN and, thereby, can be influenced by the PVN. In support of a role of the PVN in temperature regulation, we have found that neurons in the PVN projecting to the spinal cord or to the pressor region of the RVLM are activated by an increase in core body temperature (9,11). Thus, these central pathways may contribute to the central thermoregulatory pathways elicited by hyperthermia.…”

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confidence: 85%

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Role of the hypothalamic PVN in the reflex reduction in mesenteric blood flow elicited by hyperthermia

Chen¹,

Dworak²,

Wang³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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In the present study, we investigated whether the PVN is a key region in the mesenteric vasoconstriction that normally accompanies an increase in core body temperature. Anesthetized rats were monitored for blood pressure, heart rate, mesenteric blood flow, and vascular conductance. In control rats, elevation of core body temperature to 41°C had no significant effect on blood pressure, increased heart rate, and reduced mesenteric blood flow by 21%. In a separate group of rats, muscimol was microinjected bilaterally (1 nmol/side) into the PVN. Compared with the control group, there was no significant difference in the blood pressure and heart rate responses elicited by the increase in core body temperature. In contrast to control animals, however, mesenteric blood flow did not fall in the muscimol-treated rats in response to the elevation in core body temperature. In a separate group, in which muscimol was microinjected into regions outside the PVN, elevating core body temperature elicited the normal reduction in mesenteric blood flow. The results suggest that the PVN may play a key role in the reflex decrease in mesenteric blood flow elicited by hyperthermia.reflex mesenteric blood flow; increased core body temperature CARDIOVASCULAR RESPONSES TO changes in body temperature include marked changes in sympathetic nerve activity and blood flow. In response to hyperthermia, for example, there are increases in splanchnic, renal, splenic, and lumbar sympathetic nerve activity (25,28), resulting in vasoconstriction of the respective vascular beds. In contrast, hyperthermia elicits vasodilation in the skin vasculature, and in the rat tail vasodilation also occurs (21, 24); the tail is a major thermoregulatory organ in the rat. These changes contribute to the redistribution of the blood flow during hyperthermia such that blood is redirected from the warm internal environment in visceral organs to the peripheral vasculature where heat can be dissipated.The alterations in blood flow, mediated by changes in sympathetic nerve activity, involve the central nervous system. The sites in the brain that are likely to be involved in mediating the responses include the sympathetic premotor nuclei located in the hypothalamus and brain stem. These regions contain neurons that directly project to the sympathetic preganglionic motor neurons located in the intermediolateral cell column of the thoracolumbar spinal cord.Within the forebrain, the hypothalamic paraventricular nucleus (PVN) is a key integrative site involved in hormonal, endocrine, and neural control. The PVN is composed of different neuronal subgroups subserving different functions, including cardiovascular regulation. The PVN is one of the small number of premotor nuclei present in the brain (4, 47). There are neurons in the PVN that project to regions of the spinal cord where sympathetic preganglionic neurons are located and thereby can directly influence sympathetic activity (8,40,48). In addition to the spinal projecting neurons present in the PVN, there are neuronal sub...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 85%

Role of the hypothalamic PVN in the reflex reduction in mesenteric blood flow elicited by hyperthermia

Chen¹,

Dworak²,

Wang³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Descending projections from the PVN directly target the brain stem, notably the rostral ventrolateral medulla, and the intermediolateral column of the spinal cord. Through these pathways, the PVN regulates changes in systemic sympathetic activity (Shafton et al 1998;Cham and Badoer 2008).…”

Section: Discussionmentioning

confidence: 99%

TNF-.ALPHA. in Hypothalamic Paraventricular Nucleus Contributes to Sympathoexcitation in Heart Failure by Modulating AT1 Receptor and Neurotransmitters

Kang

Wang

Yang

et al. 2010

Tohoku J. Exp. Med.

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Proinflammatory cytokines, including tumor necrosis factor (TNF)-α , augment the progression of heart failure (HF) that is characterized by sympathoexcitation. In this study, we explored the role of TNF-α in hypothalamic paraventricular nucleus (PVN) in the exaggerated sympathetic activity observed in HF. Heart failure rats were made by ligating the left anterior descending coronary artery. The expression levels of angiotensin type 1 receptor (AT1-R) and neurotransmitters were analyzed in the PVN of HF rats that received direct PVN infusion of a TNF-α blocker (pentoxifylline or etanercept) or vehicle. Sham-operated control (SHAM) or HF rats were treated for 4 weeks through PVN infusion with each TNF-α blocker or vehicle. Rats with HF had higher levels of glutamate, norepinephrine, AT1-R and tyrosine hydroxylase (TH), and lower levels of gamma-aminobutyric acid (GABA), neuronal nitric oxide synthase (nNOS) and the 67-kDa isoform of glutamate decarboxylase (GAD67) in the PVN when compared to SHAM rats. Plasma levels of cytokines, norepinephrine and angiotensin II and renal sympathetic nerve activity (RSNA) were increased in HF rats. PVN infusion of pentoxifylline or etanercept attenuated the decreases in PVN GABA, nNOS and GAD67, and the increases in RSNA and PVN glutamate, norepinephrine, TH and AT1-R observed in HF rats. We have developed a novel method for chronic and continuous infusion of drugs directly into the PVN and provided evidence that TNF-α in the PVN modulates neurotransmitters and the expression of AT1 receptor, which could account for exaggerated sympathetic activity in HF.

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“…The PVN contains thermoregulatory neurons which project to the rRPa and rostral ventrolateral medulla (rVLM), important autonomic regions, to regulate sympathetic outflows to BAT and contributes to BAT thermoregulation. [43][44][45][46] Possibly, activation of H1 receptors in the PVN may stimulate the sympathetic outflow to rRPa and rVLM, which thus increases BAT thermogenesis. Collectively, this evidence suggests that histamine may increase energy expenditure via its action on H1 receptors in the PVN and POA and stimulate the sympathetic outflows to the rRPa and rVLM, therefore increasing BAT sympathetic activity and thermogenesis (Fig.…”

Section: The Role Of Histamine and H1 Receptors In Energy Expenditurementioning

confidence: 99%

The Role of Hypothalamic H1 Receptor Antagonism in Antipsychotic-Induced Weight Gain

Deng

Huang

2013

CNS Drugs

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Treatment with second generation antipsychotics (SGAs), notably olanzapine and clozapine, causes severe obesity side effects. Antagonism of histamine H1 receptors has been identified as a main cause of SGAinduced obesity, but the molecular mechanisms associated with this antagonism in different stages of SGAinduced weight gain remain unclear. This review aims to explore the potential role of hypothalamic histamine H1 receptors in different stages of SGA-induced weight gain/obesity and the molecular pathways related to SGA-induced antagonism of these receptors. Initial data have demonstrated the importance of hypothalamic H1 receptors in both short-and long-term SGA-induced obesity. Blocking hypothalamic H1 receptors by SGAs activates AMP-activated protein kinase (AMPK), a well-known feeding regulator. During short-term treatment, hypothalamic H1 receptor antagonism by SGAs may activate the AMPK-carnitine palmitoyltransferase 1 signaling to rapidly increase caloric intake and result in weight gain. During long-term SGA treatment, hypothalamic H1 receptor antagonism can reduce thermogenesis, possibly by inhibiting the sympathetic outflows to the brainstem rostral raphe pallidus and rostral ventrolateral medulla, therefore decreasing brown adipose tissue thermogenesis. Additionally, blocking of hypothalamic H1 receptors by SGAs may also contribute to fat accumulation by decreasing lipolysis but increasing lipogenesis in white adipose tissue. In summary, antagonism of hypothalamic H1 receptors by SGAs may time-dependently affect the hypothalamus-brainstem circuits to cause weight gain by stimulating appetite and fat accumulation but reducing energy expenditure. The H1 receptor and its downstream signaling molecules could be valuable targets for the design of new compounds for treating SGA-induced weight gain/obesity.

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Exposure to a hot environment can activate rostral ventrolateral medulla‐projecting neurones in the hypothalamic paraventricular nucleus in conscious rats

Cited by 18 publications

References 52 publications

Role of the hypothalamic PVN in the reflex reduction in mesenteric blood flow elicited by hyperthermia

Role of the hypothalamic PVN in the reflex reduction in mesenteric blood flow elicited by hyperthermia

TNF-.ALPHA. in Hypothalamic Paraventricular Nucleus Contributes to Sympathoexcitation in Heart Failure by Modulating AT1 Receptor and Neurotransmitters

The Role of Hypothalamic H1 Receptor Antagonism in Antipsychotic-Induced Weight Gain

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